Neuronal alterations, as a consequence of diabetes mellitus, aging, or other diseases, can cause organ dysfunciton ranging from mild to severe in scope. Urinary incontinence and erectile dysfunction are two such aspects of the human condition that may be caused by neuronal dysfunction. Each condition can have a severely adverse effect on the quality of life at great monetary expense and emotional distress to the individual. In addition to diabetes and the aging process (which affects the entire population) the neuropathies caused by stroke, Parkinson's disease, and multiple sclerosis, are examples of common illnesses that millions of people with potential bladder and penile dysfunction. We will employ the Streptozotocin (STZ) and BBAN rat diabetic models in vivo, to study the effects of diabetic neuropathy on bladder and erectile function. The effects of 1-8 months of diabetic neurepathy on bladder and erectile function be studied on consecutive days in THE SAME MALE RAT in vivo. The working hypothesis is that bladder and erectile tissue are imbued w{th significnat plasticity and that the neuronal loss, in each organ, induces a series of compensatory and/or adaptive tissue, cellular and subcellular changes. The Project, which is designed to measure the physiological effects of diabetic neuropathy, is divided into three Specific Aims. In Specific Aim #1 we will study IN THE SAME RAT ON CONSECUTIVE DAYS, the effects of diabetic neuropathy on bladder (cystometry) and erectile (cavernosometry) function, in vivo. In Specific Aim #2 we will use immunohistochemistry to study the extent of the structural changes in neural status in bladder and erectile tissue from the SAME RAT used in Aim #1; thus permitting us to directly evaluate the effects of neuronal changes on organ function in the SAME RAT. In Specific Aim #3, we will utilize microarray gene chip technologies to study diabetes-related changes in gene expression in bladder and erectile tissue obtained from animals whom have already been evaluated in Aim #1; again, permitting us to evaluate the relationship between diabetic neuropathy, organ function and gene expression.